The interactions between steroid and nonsteroid hormones in the prostate are of special interest during the growth phase of the gland. The purpose of this work is to study the influence of prolactin (PL), with or without androgenic blockade, on epithelial cells from peripubertal rat ventral prostate. Twenty male peripubertal Sprague-Dawley rats were grouped as controls, or treated with cyproterone acetate (CA), CA plus PL (CA-PL), or PL. The total number (N total) of epithelial cells, and their labeling indices to proliferative cell nuclear antigen (LI PCNA), apoptosis (LI apoptosis) and androgen receptors (LI AR) were measured. CA and PL treatment significantly decrease the N total, but the LI PCNA was unchanged. We have observed a greater LI apoptosis in pharmacologically castrated animals without PL than in the rats with androgenic blockade with PL. The LI AR does not change with CA treatment in the ventral region, but the PL significantly increases it. Androgenic blockade and PL decrease the number of epithelial cells from the ventral prostate. These changes are not attributable to the decrease of cell proliferation, rather to the increase of epithelial apoptosis. The increase of cells expressing AR after treatment with PL might be attributed to the decrease of testosterone secretion caused by the hyperprolactinemia. PL does not modulate the size of the ventral prostate in prepubertal rats. Anat Rec, 292:746-755, 2009. V V C 2009 Wiley-Liss, Inc.

Awake craniotomy is indicated for surgical resection of tumors located near eloquent areas of the brain. The anesthetic technique is based on a combination of local anesthesia, sedation, and analgesia. Usually only clinical parameters are assessed and no other cerebral oxygenation monitoring techniques are applied. The authors report the use of brain tissue oxygen pressure monitoring during awake craniotomy. A 48-year-old right-handed man with a left temporoparietal mass was scheduled for awake craniotomy, cortical stimulation, and selective tumor removal. Monitoring included electrocardiography, pulse oximetry, end-tidal CO2, bladder temperature, invasive and noninvasive arterial pressure, and brain tissue oxygen pressure (PtiO2). The anesthetic technique consisted of continuous perfusions of 0.02 to 0.05 microg/kg/min remifentanil, propofol (target concentration, 0.5 to 1.2 microg/mL), and 25 to 50 microg/kg/min esmolol, and local anesthetic blockade of the head pin insertion sites and surgical incision area (a mixture of 0.2% ropivacaine, 1% lidocaine, and epinephrine, 1:200 000). Intraoperative cortical stimulation was performed to guide the resection according to the patient's verbal response. A change in PtiO2 was observed, gradually falling from 28 mm Hg at the beginning of the intervention down to 3 mm Hg. At this stage, surgical resection was concluded. On arrival at the intensive care unit, mixed dysphasia and slight weakness of the right arm were noted. Three weeks after surgery, the patient's speech is improving and the motor deficit has disappeared. This case suggests a possible role of PtiO2 in awake craniotomy as an aid in detecting intraoperative adverse events, but further experience with PtiO2 in this setting is needed.

Abnormal angiogenesis is a critical feature of many diseases, including cancers and their precursors. Although the association between prostate carcinogenesis and changes in microvascular architecture is well known, these changes are not well-documented from a quantitative point of view. The present work deals with stereological estimates of the number of quiescent and proliferative endothelial cells, and microvessel length in normal and prostate cancer tissues. Unbiased stereological measurements of numerical densities of proliferating cell nuclear antigen immunostained cells, nonproliferating endothelial cells, caspase 3 immunoreactive endothelial cells, and relative length (length density) of microvessels, were performed in control and cancer specimens. There were no changes in either proliferation or apoptosis in carcinoma endothelial cells. A decrease of endothelial cell density, together with an increase of microvessel length density, were detected in prostate cancer specimens. Therefore, the following conclusions can be drawn: a) The increase of angiogenetic activity in prostate carcinogenesis leads to an increment of the microvascular length; b) The amount of endothelial cells per vascular length decreases in prostate cancer; c) There is no decrease of endothelial apoptosis in cancer microvessels. d) The increase of the length density of microvessels in prostate cancer is not directly associated to an enhancement of the endothelial proliferation; and e) The blood supply of epithelium was similar in both cancerous and normal prostate.

Background: Benign prostate hyperplasia (BPH) is the most common benign disease of human prostate. Currently BPH is associated with unregulated proliferation of connective tissue and glandular epithelium within the prostatic transition zone, and it has been described as relevant characteristic of BPH-the increase of the total number of cells, and not only an increase in cell size. To date, there are few studies on the quantitative morphology of glandular tree of BPH compared with normal prostate. The scarce investigations about this particular suggest that the glandular tree branches and expands as the hyperplastic transformation occurs in the prostate. Methods: To verify if this gland expansion and branching was similar to that occurs in the normal prostate, this study deals with the estimation of several stereological parameters as: labeling index for the proliferating cell nuclear antigen to quantify the rate of proliferation of prostate epithelium, average thickness of glandular epithelium, fraction of the volume occupied by the epithelium relative to the total prostate volume, connectivity density of prostate glands, to quantify the branching of prostate glands, and the average volume and the volume-weighted mean glandular volume of prostate acini to assess the mean size of the prostate acini and its variability. Results: All these estimates have been performed in prostate specific antigen immunostained sections from prostates of young men (controls) and in adenomectomy specimens from the adenofibromiomatous variety of BPH. Conclusion: We conclude that the epithelial proliferation is not the only factor intervening in the development of BPH. In addition, a more prolonged survival of epithelial * Corresponding author. L. Santamaría et al. 123 population, together with some degree of hypertrophy of acini expressed by the increase of volume fraction and thickness of acinar epithelium, is relevant in order to the growth and expansion of the BPH glandular tree that shows more abundant and heterogeneous acinar sprouts than in normal prostate.

Categorizing biologic signals by analysis of symbolic sequences was employed in the study of prostate microvessels. The estimates of the volume fraction of the vessels immunostained to Factor-VIII was mapped to binary sequences. The distance between sequences was estimated by comparing the rank and frequency of repetitive elements. These measurements were applied to detect whether there are unique microvascular patterns for each individual, and to search for patterns describing prostate microvessels of different conditions. Normal prostate, benign prostate hyperplasia and prostate carcinoma groups were studied. All the specimens were immunostained to F-VIII and strips formed by adjacent quadrats were explored. At each point of the long axis of the strip, the V(V) F-VIII was calculated. These values were processed with the information-based similarity software to estimate the dissimilarity between two space series. The following comparisons were carried out: intrasubject versus intragroup distances; intragroup distances among the groups studied and intergroup distances. The distance defined between a vessels immunostained to Factor-VIII space series and its randomized surrogate was considered as an index of the nonrandomness of the space series. These indices were compared for all the groups. We conclude that (a) The information-based similarity analysis can be adapted to vessels immunostained to Factor-VIII space series from prostate microvessels. (b) There are no unique microvascular patterns associated with each individual. (c) There are characteristic patterns describing the microvessels from normal prostate, benign prostate hyperplasia and carcinoma. (d) This method is able to account for the differences between prostate cancer and both normal and benign prostate conditions, with respect to the microvessel patterns.

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This work deals with the quantification of serotonin-immunoreactive prostate neuroendocrine cells (NECs) in rats exposed to prolactin in normal, cyproterone acetate-exposed, and bromocriptine-exposed animals to establish the possible influence of prolactin with or without androgenic blockade on this cell population. Thirty male peripubertal Sprague-Dawley rats were grouped as controls (CT) and those treated with cyproterone acetate (CA), cyproterone acetate plus prolactin, cyproterone acetate plus bromocriptine, prolactin (PL), and bromocriptine (BC). The volume of ductal epithelium (Vep) and total number (NSER) of the NECs serotoninimmunoreactive were measured. NECs were detected in the periurethral ducts. Compared to CT, Vep was increased in PL and BC and NSER was decreased in CA and increased in the prolactin or bromocriptine groups. The androgenic blockade decreases NSER in rat prostate; PL induces in normal and cyproterone acetate-treated rats the increase of NSER; and BC exerts a local effect over the prostate similar to that described for PL.

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